SAT-326 - A Wellness Trend Gone Awry: Cold Plunge Leading to Thyrotoxic Periodic Paralysis

Introduction
Thyrotoxic periodic paralysis (TPP) is a condition characterized by episodic paralysis due to thyrotoxic induced hypokalemia, that resolves with treatment of thyrotoxicosis. TPP is commonly due to Graves’ disease, is more frequent in Asian males, and a specific trigger is identified in one third of instances. This case highlights a patient with TPP that was precipitated by a cold plunge.

Case Description
A 39-year-old previously healthy male from Nepal presented with acute left sided paralysis in the setting of months of muscle cramping and lower extremity weakness. He reported a 30-pound weight loss over several months, tremors, and frequent bowel movements. He did not take any medications or supplements and no significant alcohol or substance use. His family history was notable for a sister with Lupus. He was hospitalized a month prior for hypokalemia and was discharged with a few days of oral potassium replacement. The day prior to the onset of muscle weakness, he consumed an alcoholic beverage and participated in a cold plunge. On admission, the patient was bradycardic with a heart rate of 27 and an EKG showed second degree AV block. His heart rate normalized with atropine administration. Physical exam was notable for a diffusely enlarged, non-tender thyroid gland, smooth skin and fine tremor with outstretched arms. There was no exophthalmos. Laboratory workup revealed a potassium of 1.6 mmol/L (3.5-5.3), magnesium 1.8 mg/dL (1.5-2.5), CK 53 U/L (30-223), TSH < 0.01 mIU/L (0.45-4.12), free T4 2.66 ng/dL (0.61-1.76), total T3 253.9 ng/dL (60-220), thyroid peroxidase antibody 270 IU/mL (0-9), TSH receptor antibody (TRAb) 7.53 IU/L (0-1.75), and TSI 16.6 IU/L (0-0.55). Thyroid ultrasound showed an enlarged, heterogenous thyroid gland with hyperemia. Positive thyroid autoantibodies confirmed hyperthyroidism from Graves’ disease as the cause of thyrotoxicosis leading to TPP. Acutely, potassium supplementation was required to prevent recurrence of paralysis but was no longer needed as hyperthyroidism responded to treatment with methimazole.

Discussion:
This case illustrates a unique trigger for TPP in a patient with previously undiagnosed Graves' disease. In the absence of other recognized triggers such as trauma and infection, the cold plunge likely contributed to the current presentation. Cold exposure can provoke the release of catecholamines, thereby exacerbating existing thyroid hormone activation of Na+-K+-ATPase. As potassium moves intracellularly, hypokalemia-mediated muscle paralysis ensues. Although this mechanism is established, to our knowledge, this case is the first to describe a cold plunge precipitating TPP as the initial presentation of Graves’ disease in a young Nepalese male. Cold plunges are becoming increasingly popular as a wellness trend and should be recognized by clinicians as a potential contributor to this serious but treatable condition.

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